Translational Research: Multi-Scale Models of the Pulmonary Circulation in Health and Disease - Multiscale Computer Modeling in Biomechanics and Biomedical Engineering - page 275

Fig. 7 Predicted acinar
a perfusion, b ventilation-
perfusion ( V/ Q) ratios and
c alveolar oxygen partial
pressures (P AO2 ) in a subject
with 40 % tissue occlusion by
7 mm pulmonary emboli.
Black regions in b are areas
with V/ Q [ 1 (more
ventilation than perfusion)
and in c are areas with
P AO2 \ 80 mmHg (hypoxic).
This figure was first published
in Pulmonary Circulation
[ 34 ]

pronounced in the gravitationally non-dependent lung, which normally receives
the least blood flow so has a greater capacity to carry more blood when the lung is
under stress. In the absence of an underlying pathology, the small increases in PAP
predicted by a model of mechanical occlusion alone [ 33 , 34 ] suggests a significant
role for active mechanisms in determining response to PE.
Burrowes et al. [ 34 ] incorporated the model of oxygen exchange described by
Eqs. 9 and 10 to investigate the possible role of hypoxia in PE. They found that
localized hypoxia was predicted in non-occluded regions following arterial
occlusion (Fig. 7 ), as well as a significant reduction in oxygen levels in the blood
that returns from the lungs to the systemic circulation. Localized hypoxia may be
significant in elevating PAP in PE, with pulmonary vessels actively constricting in
hypoxic conditions. Constriction of small pulmonary vessels in non-occluded
regions in PE may act to restrict the ability of the lung to redistribute blood flow,
and so elevate blood pressures required to maintain cardiac output. However, the
redistribution of blood away from hypoxic regions may have the beneficial effect
of improving

V/ Q matching and so the efficiency of the diseased lung for gas

exchange.
An alternative, or additional, mechanism for increased PAP in response to PE is
the response to increased cardiac output. Experimental [ 95 - 97 ] and modeling [ 34 ,
87 , 98 ] studies agree that PAP increases more rapidly than cardiac output in PE
than under normal conditions. Tawhai et al. [ 87 ] used estimates of metabolic rate